The invention relates generally to cardiopulmonary resuscitators and, more particularly, to an improved CPR protocol and cardiopulmonary resuscitator for affecting the same.
External cardiac compression can effectively be employed for obtaining perfusion by causing forced pumping of blood from a temporarily stopped heart. This is normally achieved by constant cyclic external compression of the heart (systole) for a short time period followed by pressure release to allow heart expansion (diastole) for a short time period. To achieve proper heart compression by external force, the breast bone is forced toward the backbone of the patient while the patient's back is rigidly supported.
Although forced pumping of blood is essential for a patient whose heart has stopped, this is only part of the continuous treatment necessary, since when the heart stops, breathing stops also. Hence, when external mechanical or manual cardiac compression is presently employed, simultaneous sustained cyclic mechanical or mouth to mouth ventilation is also important to cyclically inflate the lungs for oxygenization of the blood. According to accepted medical practice, the lungs are ventilated or inflated during the diastole period of the compression cycle. Whether carried out mechanically or manually, these techniques comprise what is commonly referred to as cardiopulmonary resuscitation or CPR.
The operating theory behind current CPR protocol is that cardiac compression produced by physical compression of the heart between the sternum and the spine of the patient, pressurizes the chambers in the heart driving blood through the one-way valves of the heart and through the vascular beds in the normal direction. During this process, the left side of the heart supplies oxygenated blood to the patient's body through the arterial system and the right side of the heart perfuses blood by directing blood through the pulmonary bed and back to the left heart. More recent findings however indicate that this is only an infrequent mechanism for perfusion and that the anatomy of an individual is important as to whether this mechanism works. Only patients with fairly large hearts and fairly small chest dimensions actually receive perfusion by this mechanism and data would indicate that this occurs in only twenty to thirty percent of patients. An alternate theory has developed to the effect that generally high intrathoracic pressures during external cardiac compression may be the primary mechanism for driving blood through the heart. Since intrathoracic pressure, or the pressure within the chest cavity defined by the rib cage, is also influenced by pressure within the patient's lungs, the mechanics of ventilation have become very important in producing perfusion. In particular, it has been found that by inflating the lungs during chest compression to fairly high pressures, that cardiac output is greatly enhanced.
This theory would explain recent developments such as "cough" CPR. During a typical cough, very high intrathoracic pressures are produced, and it has been found that blood is perfused by these high intrathoracic pressures created only by high pressures developed in the lungs and thorax by the muscle and valving action of the body during the act of coughing. And indeed, it has been demonstrated that cyclic coughing is a suitable technique for keeping a patient viable who has gone into ventricular fibrillation. As long as the patient can cough regularly, he can maintain himself in a viable state and conscious until help arrives. Of course, cough CPR is merely supportive therapy and definitive therapy such as defibrillation has to be applied quickly to save the patient. Cough CPR is only a very temporary procedure.
Others have found that ventilating intubated patients during every systolic period of CPR with relatively high pressures on the order of 100 to 150 centimeters of water greatly enhances cardiac output and yields adequate blood gases. Normally, these are considered dangerously high pressures that alone would cause trauma to the lungs. However, it has been found that when these ventilating pressures are precisely synchronized with the systolic portion of the chest compression cycle, the generally high intrapulmonary pressures are equalled by the intrathoracic pressures and there is no substantial difference of pressure across the alveoli. Thus, these relatively high ventilator pressures are regarded as safe if applied simultaneously with cardiac compression. In connection with this technique, observations have been made that the heart valves are frequently incompetent and therefore some other valving mechanism has to be found to account for the forward perfusion of blood. This is especially true for cerebral perfusion since all of the pressures acting on the vessels within the thoracic cage are basically identical. That is, central venus pressure is equal to aortic pressure which is equal to intrathoracic pressure. In connection with this, it has been observed that the veins leaving the thorax apparent collapse under these conditions and this creates a valving action, preventing retrograde venus flow through the upper main veins such as jugular vein, whereas the arterial lines stay open so that some blood is pushed into the arterial bed without an equivalent retrograde venous flow. Thus, it is apparently possible to create forward perfusion without the working of the cardiac valves. Problems with this CPR protocol involve the use of very high ventilation pressures which are not easily obtained with conventional resuscitators. Also, since the pressure used for ventilation is dangerously high, as a differential alveolar pressure, the application of these ventilation pressures must be precisely synchronized with elevated thoracic pressure during systole. For example, should the force on the chest be inadvertently reduced or should external cardiac massage be momentarily interrupted during ventilation, an extremely dangerous pulmonary differential pressure would be reached which might well be traumatic to the lungs. Furthermore, despite the use of high ventilation pressures with this technique, there is no certainty of the adequacy of established pulmonary differential pressures which are a measure of tidal volume needed to establish adequate gaseous exchange and to reduce atelectasis. That is to say, while this CPR technique would appear to improve the pumping of blood through the heart it has not always adequately oxygenated the patient's blood.
Another proposed technique for employing ventilation to enhance perfusion has involved using relatively benign ventilator pressures such as 20 to 30 centimeters of water. According to this technique, once external cardiac massage is established, this relatively benign ventilator pressure is applied to the lungs for three complete compression cycles and then the patient's lungs are vented to the atmosphere for two complete compression cycles in a continuous fashion. Although this technique has been found to enhance cardiac output and yield good blood gases, problems encountered with this CPR protocol include the fact that intrathoracic pressures are limited by forward ventilation pressure since retrograde or exhale flow is possible out ventilator control valves during chest compression. This severely limits pressure buildup in the lungs during the application of external cardiac massage and creates a limitation on cardiac output. Also, with this technique there of course would be no enhancement of intrathoracic pressure during the exhale period of the ventilatory cycle.